Maternal Diabetes Mellitus (DM) is recognized to predispose the arterial and venous thrombosis in the neonate. The pathogenesis of this complication in the infant of the diabetic mother (IDM) is speculative. In the adult with DM, abnormalities in the metabolism of arachidonic acid (AA) by the platelet and vessel wall occur, which lead to an increase in the production of proaggregatory platelet Thromboxane A2 (TxA2), and a decrease in antiaggregatory vascular PGI2. This imbalance may play a role in the evolution of diabetic angiopathy. The main purpose of our project is to ascertain whether the increased incidence of thrombosis in IDM is associated with an imbalance in platelet-vascular AA metabolism. If an imbalance (an increase in TxA2 and/or a decrease in PGI2) is observed, the time period during which these abnormalities persist will be documented. In vitro studies will also be performed to elucidate whether the changes in AA metabolism are intrinsic to the tissues studied, or due to extrinsic plasma factor(s). Platelet AA release and metabolism to TxB2, HHT, and HETE will be evaluated in control and diabetic pregnant women, during pregnancy, at delivery, and post-partum. Sequential evaluation of plasma and urine for 6 Keto PGF1 alpha (the end product of vascular PGI2) will also be performed. At the deliveries of the subjects evaluated above, cord blood will be obtained for similar studies. If differences occur in the IDM when compared to control infants, venous blood will be obtained neonatally to document the period of persistence of the abnormalities. It is anticipated that differences in AA metabolism if present, will be defined by such an approach. A secondary goal will be an attempt to correlate the presence of abnormalities with various factors i.e. blood sugar, cholesterol, HDL, LDL, growth hormone, somatomedin, circulating platelet aggregates, or maternal levels of Hb.A1c.